We propose to study the mechanism by which an IgA myeloma tumor, MOPC-315-EL (BALB/c origin), undergoes a periodic loss, during each transplantation cycle, of the ability to interact with thymus-derived lymphocytes (T). Our approaches will center around the evaluation of the T lymphocyte-tumor cell interaction and the structural change(s) which is responsible for the altered reactivity. The cellular interactions between T cells and the reactive and unreactive MOPC-315-EL tumor cells will be evaluated by 1) T lymphocyte-tumor cell conjugate formation, 2) inhibition of T cell-tumor cell conjugate formation with solubilized, enriched H-2 antigen containing fractions from the reactive and unreactive MOPC-315-EL tumor cells, and 3) by the ability of the solubilized H-2 containing fractions from the reactive and unreactive tumor cells to elicit specific cytotoxic T lymphocytes (CTLs) in culture. Structural changes which might be responsible for the reduced T cell reactivity will be studied by examination of the surface protein, lipid, and carbohydrate composition of the reactive and unreactive MOPC-315-EL tumor cells. A study of the in vivo relationship between the host (BALB/c mouse) and the tumor will be carried out by establishing 1) whether there exists heterogeneity of the MOPC-315-EL tumor cell population, 2) whether a soluble factor is responsible for the induction of the change in reactivity of T cells, and 3) whether this change in reactivity to T cells is an important tumor escape mechanism.